Download to read offline
More Related Content
Similar to Dermatological Emergencies: What should be known
![dermatological emergencies [Autosaved] [Autosaved].pptx](https://cdn.slidesharecdn.com/ss_thumbnails/dermatologicalemergenciesautosavedautosaved-250718141557-4ff0fe21-thumbnail.jpg?width=640&height=640&fit=bounds)
Dermatological Emergencies: What should be known
- 1. 1 DERMATOLOGICAL EMERGENCIES Sunil Timilsina 1st year PGResident GP and EM NAIHS
- 2. Outline • Introduction • Conditionsresulting in dermatological emergencies • References 1
- 3. Introduction • Dermatological emergenciesare those cutaneous conditions that can be life threatening if not diagnosed quickly and managed accordingly. • Dermatological conditions with widespread systemic involvement and complication are the emergencies that have to be dealt with in ER. • Prompt recognition for appropriate diagnosis and treatment is necessary to improve a patient’s prognosis and a single decision can make the difference between LIFE and DEATH. • Multiple faculties involvement according to the emergency of the condition is required. 2
- 4. Conditions resulting in Dermatological Emergencies 1.Erythoderma 8.Bacterial Toxin Mediated Illnessess - Staphylococcal Scalded Skin Syndrome -Toxic Shock Syndrome 2. Anaphylaxis 9. Drugs induced Cutaneous Necrosis Warfarin/Heparin/Vasopressors 3. Severe Cutaneous Drug Reactions 10. Vesiculobullous disorders -Pemphigus Foliaceus 4. Psoriasis - Psoriatic Erythroderma - Acute generalized pustular Psoriasis 11. Vascular disorders 5. Leprosy Reactions 12. Acute Graft Vs Host Disease 6. Erythema Multiforme 13. Metabolic Disorders -Pellagra - Acrodermatitis Enteropathica 7. Infections 3
- 5. Erythroderma • Erythroderma isan inflammatory skin disease with redness and scaling that affects 90% or more of the patients skin. • Also known as Exfoliative Dermatitis • Extensive skin exfoliation : 20-30g/day • 18-20% mortality • Males affected more (4x) 4
- 6. Presentation • Initial lesions •Erythema – rapidly progressing later scaling • Established Case • Erythema, Scaling and Induration involving >90% BSA • Ectropion, Eclabium, Everted nostrils and flexion contracture of joints • Later • Exagerrated skin folds and shedding of hair, eyebrows, eyelashes and nostrils • Lymphadenopathy • Association : Extreme pruritus, Enteropathy, • Lesion of primary illness 5
- 7. Why an Emergency? •Temperature Dysregulation • Skin loss and hypothermia • High Output Cardiac Failure • Dehydration and Electrolyte imbalance • Hypoalbuminemia • Loss of muscle mass • Thrombophlebitis/DVT • Infection-both cutaneous and respiratory with pneumonia a major cause of death 6
- 8. Causes Diagnostic CluesAssociated features Ichthyosis and related syndromes Present since or soon after birth. Adherent scales. May have positive family history Psoriasis Typical psoriasiform plaque Nail changes Pityriasis pilaris rubra Islands of Normal Skin. Salmon colored erythema Orthokeratosis, Parakeratosis Inflammatory disorders Atopic Dermatitis Fulfilling diagnostic criteria History of atopy Seborrheic Dermatitis Yellowish greasy scale involving seborrheic areas History of recurrent seborrheic dermatitis Airbrone Contact Dermatitis Prior history of contact dermatitis Causes 7
- 9. Causes Diagnostic CluesAssociated features Pemphigus Foliaceous Superfical erosions with collarette of scales +ve Nikolsky sign Subcorneal split in HPE SSSS Skin tenderness +ve Nikolsky sign Norwegian Scabies Intense pruritus in background of immunocompromised states Mite under microscope Drug Hypersensitivity Syndrome Systemic involvement History of drug intake Sezary syndrome Leonine facies in long standing cases Sezary cells in PBS Dermatomyositis Heliotrop rash, Poikiloderma, Gottron’s papules, proximal muscle weakness Raised muscle enzymes Sarcoidosis Ichthyosiform erythroderma Sarcoidal granuloma in HPE Causes 8
- 10. Investigations • CBC,RFT withelectrolyte, LFT, blood culture, RBS • Skin swab-microscopy and culture sensitivity • Chest x-ray • Skin biopsy-if cause uncertain 9
- 11.
- 12. 11 Condition Clinical pictureTreatment Anaphylaxis • Intense pruritus • Flushing • Stridor • Hypotension Shock • Adrenaline • Respiratory Support • Antihistaminic • Steroids Utricaria • Intense pruritus • Localized wheals • Triggerer avoidance • Emollients • Antihistaminic • Leukotriene antagonists • Steroids • Immunotherapy Angioedema • Swelling of face/lips/peri orbital region
- 13.
- 14. Acute Generalized PustularPsoriasis • Occurs in patients with any variant of psoriasis • Due to any provocating factors • Most commonly after sudden withdrawal of topical or systemic steroids. 13
- 15. Why an Emergency? •Severe hypoalbuminemia • Hypocalcemia and tetany • Oligemia and Acute tubular Necrosis • Malabsorption • Deep vein Thrombosis and Pulmonary Embolism 14
- 16. Clinical Presentation • Generalizedpustular eruptions with “lake of pus” formation • Intense burning sensation, erythema • Skin tenderness • Fever • Repeated crops of lesions • May develop erythroderma 1
- 17. Investigations • Basic laboratoryprofile • Gram staining of smear from pustules PMN cells without organism • Skin biopsy 16
- 18. Management • DICU admission •General Measures • Mild sedation • Fluid and electrolytes • High protein diet • Systemic Therapy: • Acitretin 1mg/kg/day to overcome acute stage and then 0.5 to 0.75mg/kg/day to control • PUVA therapy • Acetretin + PUVA • Methotrexate IV/IM 0.3mg/kg/week • High dose cyclosporine (9-12 mg/kg/day) • Parenteral corticosteroids 17
- 19. Erythema Multiforme • Acute,usually mild, self-limited cutaneous and/or mucocutaneous syndrome • Types: EM major: mucous membrane involved EM minor: mucous membrane not involved • Causes: Infection (mostly): HIV,HSV, Mycoplasma Drugs: Uncommon 18
- 20. Clinical features • Rapidonset of lesions within few days, • Mild pruritic or painful papular or urticarial lesion- Target lesion • Oral mucosa: ulcers, erosion, difficulty swallowing Oesophageal stricture • Eye-permanent eye damage • Urethra-stricture and urinary retention • Sepsis, cellulitis, permanent skin damage & scarring • Inflammation of internal organs-lungs, liver 19
- 21. Investigation • CBC, CRP,RFT with electrolytes, LFT with enzymes • Biopsy: If diagnosis uncertain • Swabs: HSV PCR • Imaging: Chest X-ray PA view • Serology: Mycoplasma (if respiratory symptoms present) 20
- 22. Treatment • Treatment ofunderlying cause • Withdrawl of any causative agent • Symptomatic treatment-analgesics, antipyretics, topical steroids, antihistamine • Xylocaine and diphenhydramine elixir for oral ulcers • Consider Ophthalmology consultation if eyes involved • Consider medicine consultation if systemic organ involvement • Liquid diet • I/V fluid therapy and electrolyte replacement • Antibiotics if secondary infection suspected • Tab. acyclovir 800mg 5 times a day for 7 days • Consider systemic steroid use • Admit for further treatment 21
- 23. Severe Cutaneous DrugReactions • High mortality • Common in extremities of age • Women more susceptible than men • Includes: • SJS/SJS-TEN overlap/TEN • Drug Reaction with eosinophilia and systemic symptoms • Serum Sickness • Acute generalized Exanthematous Pustulosis 22
- 24. 23 Condition Mechanism ClinicalPicture Treatment Remarks SJS/SJS- TEN/TEN Type IV hypersensitivity reaction • Initial Prodrome • Painful erythematous macules of targetoid appearance • +ve Nikolsky sign • Drug discontinuation • Fluid Resuscitation • Wound care • Topical steroids • IV Ig 1-2 mg/kg/day x 3- 4 days SJS: <10 % BSA SJS-TEN: 10-30% BSA TEN: > 30%BSA SCORTEN scoring for severity DRESS Not fully understood • Initial Prodrome • Generalized morbilliform pruritic rash with cephalo caudal progression • Systemic involvement • Drug discontinuation • Severity assessment • Adequate Hydration • Wound care • Topical and systemic steroids • Immunosuppre sants 2 forms: • Non serious - no organ involvement or stage 1 AKI or mild liver injury • Serious - stage 2 AKI or severe liver injury or other system involvement
- 25.
- 26. 25 Condition Mechanism ClinicalPicture Treatment Remarks Serum Sickness Type III hypersensitivity reaction Triad of • Fever • Arthralgia • Skin rash • Discontinuation of drug • Antihistamines • NSAIDS • Systemic Steroids Occurs by 2 weeks after exposure to drugs Acute Generalized Exanthematous Pustulosis T cell mediated neutrophilic inflammation • rapid development • dozens to hundreds nonfollicular, sterile, pinhead-sized pustules on a background of edematous erythema with flexural accentuation • Drug withdrawal • Supportive care Symptomatic treatment • Pruritus and skin • inflammation: Medium Potency topical steroid • Desquamation phase: Emollients Resolves spontaneously in 1-2 weeks after stopping drug
- 27. 26 AGEP AGEP withflexural accentuation Serum Sickness
- 28. Drugs induced CutaneousNecrosis Drug Mechanism Clinical Picture Why an Emergency? Management Warfarin transient hypercoagulable state during initial warfarin administration that in turn leads to vascular occlusion and tissue infarction followed by extravasation of blood. • demarcated areas of purpura and necrosis • Starts within D1- D10 • Symmetrical Extensive area of necrosis may lead to acute skin failure • Discontinuation • Heparin • Vit. K IV • FFP or Protein C concentrate transfusion • Supportive Measures Heparin • Antigen Antibody complex formation • Incorrect injection technique • Persistence on subcutaneous tissue • Manifests within first two weeks • Well demarcated erythema, edema, pain • Bullae formation and necrosis Rapid progression • Discontinuation • Switch to non- heparin anticoagulant • 4t score calculation and management 27
- 29. 28 Heparin Induced skin necrosis Necrosisalong peripheral line by nor-adrenaline
- 30. Drugs induced CutaneousNecrosis 29 Drug Mechanism Clinical Picture Why an Emergency? Management Vasopressor • Excessive vasoconstriction with inadequate circulating volume • Immunological Phenomenon • Ecchymotic area which soon changes to black along the line of vasopressor infusion • Extensive tissue loss • Rapid progression • Discontinuation • Increasing preload • Analgesics • Topical nitroglycerine • Inj. Phentolamine 5mg • Surgical debridement
- 31. Metabolic Disorders Cause PathophysiologyClinical Picture Management Acrodermatitis Enteropathica • Intestinal absorption defect due to defective intestinal zinc transporter protein • Autosomal Recessive • erythematous and vesiculobullous dermatitis • Alopecia • Ophthalmic manifestations • Severe growth retardation • Recurrent infections • To measure fasting plasma zinc level • < 60mcg/dl • 3 mg/kg/day of elemental zinc (13.2 mg/kg/day of zinc sulfate or 10.1 mg/kg/day of zinc acetate) • Lifelong zinc supplementation 30
- 32. Metabolic Disorders 31 Cause PathophysiologyClinical Picture Management Pellagra • Deficiency of Niacin • symmetric hyperpigmented rash, similar in color a distribution to a sunburn. • present in the exposed areas of skin. • "Casal necklace“ appearance • Diarrhea • Neuropsychiatric symptoms • Food fortification • Niacin supplementation • Supportive care
- 33. Norwegian Scabies • Seenin immunocompromised individuals • begins with poorly defined, erythematous patches that quickly develop prominent scale • usually spreads inexorably and may eventually involve the entire integument • Scales become warty, especially over bony prominences. • Crusts and fissures appear. • The lesions are malodorous. • Nails are often thickened, discolored, and dystrophic. • Pruritus may be minimal or absent. 32
- 34.
- 35. Why an Emergency? •Associated fissures provides entry point for organism • Secondary infection • Septicemia • Glomerulonephritis • Aesthetic complications 34
- 36. Management • United StatesCenters for Disease Control and Prevention's combination regimen for the treatment of crusted scabies: • Permethrin 5% cream applied every two to three days for one to two weeks • and • Oral ivermectin (200 mcg/kg/dose) given for three, five, or seven nonconsecutive days depending on severity of infestation • Second generation antihistaminics for pruritus 35
- 37. Pemphigus Foliaceous Epidemiology AutoantigenC/F HPE DIF IIF ELISA Variants • Middle aged adults • Endemic form common in children and young adults Desmoglein 1 • Fragile blisters • Shallow erosions • Erythema tous crust • Absent mucosal involvem ent • Positive nikolsky sign Subcorneal or granular layer acantholysi s Intercellular IgG deposition Circulati ng IgG DSG 1 autoanti bodies • Fogo sevalgem • Senar Usher syndrome 36
- 38. Treatment 37 No Yes Rituximab therapy feasible? To startPrednisolone 0.5- 1mg/kg/days And Rituximab To start Prednisolone 0.5- 1mg/kg/days Add MMF or AZA Disease control achieved within 1 month?
- 39. 38 Patient treated withrituximab Disease control achieved within 1 month? Patient not treated with rituximab Increment of prednisolone upto 1.5mg/kg/day • Increment of prednisolone upto 1.5mg/kg/day • Switching immunosuppressant • Rituximab to be considered Disease control achieved within 1 month? No MMF or AZA or treat as refractory PF Tapering prednisolone after achieving stable disease control If replase occurs: • Rituximab administration if not given previously or last dose: 4-6 months • MMF or AZA to be added if prednisolone or rituximab insufficient • Switching immunosuppressant if already on it Yes Yes No No Ref: Joly P, et.al. Updated S2K guidelines on the management of Pemphigus Vulgaris and Pemphigus Foliaceous by EADV. J Eur Acad Dermatol Venerol 2020; 34:1900 Yes
- 40. Lepra Reactions Type 1(reversal)Type 2(ENL) Lucio phenomenon Mechanism Delayed hypersensitivity possibly immune- complex deposition Cutaneous vasculitis probably due to immune-complex deposition Diseases Borderline(BT,BL) Lepromatous (BL,LL) Cutaneous lesions Erythema, edema and scaling of previous lesions Appearance of – several tender, evanescent erythematous nodules on face, flexures, legs, which sometimes becomes pustular Large, sharply marginated, ulcerative lesions that appear in crops over the lower limbs and may recur episodically Neuritis Common and severe Common and severe Not common 39
- 41. Lepra Reactions Type 1(reversal) Type2(ENL) Lucio phenomenon Systemic Manifestations Not common Fever, malaise, Arthralgia, tender lymphadenopath y, orchitis, acute uveitis, glomerulonephri tis Not common Treatment Mild: NSAIDS Mod: NSAIDS and or Prednisolone Severe: NSAIDS and Prednisolone (for up-to 18 months depending upon severity) Mild: NSAIDS Mod: NSAIDS, Prednisolone Severe: NSAIDS,Prednisol one, High dose Aspirin Supportive Prednisolone 40
- 42.
- 43. Bacterial Toxins MediatedIllness 42 Staphylococcal scalded Skin Syndrome Toxic Shock Syndrome Cause d/t exfoliative toxin A and B TSS-1 toxin and super antigens of Staph. Aureus (MRSA) GAS organism Skin involvement Yes Yes Mucous involvement No Yes Multisystem Involvement No Yes Prognosis Good Poor Treatment Good skin care Antibiotics (Iv preferred) Anti-Shock therapy Surgical debridement Antibiotic therapy
- 44.
- 45. 44 Condition Mechanism ClinicalPicture Treatment Remarks Kawasaki Disease Multifactorial • Fever • Conjunctivits • Skin rash • Oral mucositis • Polymorphous rash • Cervical lymphadenopathy • Erythema, induration & or desquamation of extremities • IV IG • Aspirin • Steroids • Supportive measures 6mo-5yrs commonly affected Boys more affected Purpura Fulminans Congenital or Acquired deficiency of Protein C/ protein S/ anti thrombin III • Ecchymoses • Areas of Skin necrosis • FFP • Protein C concentrate • Anticoagulants 3 variants a) Idiopathic b) Neonatal c) Acute Infective
- 46.
- 47.
- 48. Acute Graft VsHost Disease • due to inflammatory immune cell infiltrate involving T cells, macrophages, monocytes and neutrophil granulocytes with associated tissue destruction and apoptosis • After allogeneic hematopoietic cell transplant (HCT) 47
- 49.
- 50. Clinical Picture • maculopapularrash • Blanchable erythema • Initially nape of neck, face and extremities later becomes generalized • Pruritic and or painful • persistent nausea and/or emesis • abdominal cramps with diarrhea (bloody) • rising serum bilirubin concentration 49
- 51. Why an Emergency? •Multisystem involvement • Marked thrombocytopenia • ~50% chance of mortality in severe form 50
- 52. Management • Based onthe severity • General Measures plus • Grade 1: • Topical steroids • Topical 0.1% Tacrolimus • Oral Roxulitinib • Gardes ≥2 : Systemic steroids • Methylprednisolone 2mg/kg/day in divided doses • Oral Roxulitinib 10mg BD 51 Resistant cases
- 53. Bacterial Infections Disease ClinicalFeature Investigations Why an Emergency? Cellulitis • poorly defined lesion with induration • erythema, edema, warmth, tenderness • Basic lab profile • Rapid progression • Septicemia NSSTI • diffuse erythema, edema • crepitus, skin necrosis, • Ecchymosis • signs of systemic toxicity. • Basic lab profile • CPK raised • Deep tissue culture • Rapid progression • Limb Amputation • Sepsis • DIC • Death 52
- 54.
- 55. 54 Bacterial Infections Disease ClinicalFeature Investigations Why an Emergency? Abscess • Painful, tender, and fluctuant red swelling • May have surrounding erythema and induration • Basic lab profile • Rapid progression • Septicemia
- 56. Signs of skinand soft tissue infection? Signs of necrotizing infection? Yes 1. Emergency surgical debridement + Tissue culture and sensitivity 2. Empiric IV antibiotics • Daptomycin OR linezolid OR Vancomycin plus • Carbapenam OR Piperacillin/tazobactam, OR Fluoroquinolone+Metronidazole OR Ceftriaxone + Metronidazole No Non-purulent infection Cellultis Purulent infections Abscess Severity determination PE, labs ± Imaging TREATMENT 55
- 57. Severity determination PE, labs± Imaging Mild infections Locally confined Oral Antibiotics: • Cephalexin • Flucloxacillin • Dicloxacillin • Clindamycin Incision and Drainage only Topical Antibiotics to be considered Moderate infection systemic involvement IV antibiotics • Penicillin • Ceftriaxone • Cefazoline • Clindamycin Incision and Drainage with Culture and sensitivity Oral/IV antibiotics: • TMP/SMX • Doxycycline • Flucloxacillin Contd… 56
- 58. Severe infection • Failedinitial treatment • SIRS • Immunocompromised • Features of necrosis IV antibiotics: • Vancomycin PLUS • Piperacillin/tazobactam OR Meropenam Surgical Debridement + Culture and sensitivity Incision and drainage with culture and sensitivity IV antibiotics: • Vancomycin • Daptomycin • Linezolid • Telavancanin • Ceftaroline • Specific antibiotic therapy as per culture and sensitivity reports • To evaluate and treat risk factors for recurrent infections Contd.. 57
- 59. 58 Condition Mechanism ClinicalPicture Treatment Herpes Zoster Ophthalmicus reactivation of VZV in the ophthalmic division of the trigeminal nerve • Prodrome • Pain • Vesicles formation • Conjunctivitis/Uveitis/ Keratitis Rest and Hydration • Acyclovir 800ng IV or PO 5 times/d x 1-3 weeks • Cyclopegics • Steroids Herpes Zoster Oticus reactivation of VZV in the geniculate ganglion, affecting the seventh (facial) and eighth (vestibulocochlear) cranial nerves • Prodrome • Vesicles in EAC • Ipsilateral CN VII paralysis • Otalgia • SNHL • Vertiogo ± • Rest and Hydration • Acyclovir 800ng IV or PO 5 times/d x 1-3 weeks • Prednisolone 1mg/kg/d 1-3 wks • Amitryptilline for neuralgia Viral Infection
- 60. 59 Ramsay Hunt Syndrome Herpeszoster ophthalmicus
- 61. References • Textbook ofAdult Emergency Medicine-5th edition-Peter Cameron • Critical Care in Dermatology 2nd edition – Jaypee Publications • Uptodate 1
- 62.
Editor's Notes
- #4 Acute Skin Failure-by Irvine(1991) loss of normal temperature control with inability to maintain core body temperature and failure to prevent percutaneous loss of fluid, protein with resulting imbalance, and failure of mechanical barrier to prevent p-enetretation of –foreign materials
- #5 Normal : 0.3g/day
- #6 Scaling after 2-6 days Over Flexure surface
- #8 Alternating O and P oriented in horizontal and vertical directions
- #19 Type IV
- #24 Sjs begins within 1-3 weeks of drug intake DRESS onset 2-8 weeks DRESS: type IV hypersensitivity rxn or primary infection or reactivation of HHV_6
- #28 Higher dose of warfarin= 10mg or more
- #31 Corneal scarring, cataract, retinal detachment, and optic atrophy
- #36 (approximately days 1, 2, and 8; approximately days 1, 2, 8, 9, and 15; or approximately days 1, 2, 8, 9, 15, 22, and 29)
- #38 Initial dose: IV: 1 g once every 2 weeks for 2 doses in combination with a systemic glucocorticoid, followed by a maintenance dose Maintenance dose (if complete remission is achieved with initial therapy): IV: 500 mg once 12 months after initial therapy, then every 6 months thereafter or based on clinical evaluation, but no sooner than every 16 weeks
- #39 Disease control : point of cessation of new lesion formation and established lesions begins to heal Prednisolone tapering started after disease has been stable for 2 weeks and 80% established lesions have started to heal
- #50 Acute: within 100 days Hyperacute: within first 2 weeks Late onset: after 100 days
- #52 Monitoring for cytopenias
- #57 Oint.Mupirocin Oint. Retapamulin
- #58 IDSA SIRS definition: HR>90;RR>24;temp>38 C; abnormal WBC Vanco:15mg/kg q 12hrs Dapto: 4mg/kg q 24hr Tela:10mg/kg OD Cefta: 600 mg BD Line:600 mg BD